The precise modes of human immunodeficiency virus (HIV) infection in infants are not completely understood, but both in utero and perinatal infection have been documented, with an estimated incidence in infants born to HIV-infected mothers of 20-50%. The clinical disease syndrome observed in HIV-infected infants differs significantly from that seen in infected adults. Although some infected children remain asymptomatic for 7-10 years or more, the interval prior to the onset of disease is usually less than 1 year and the clinical course is often rapidly fatal. Limited studies of virus genotypes in HIV-infected mother-infant pairs have shown that infants are most often infected with one or a few viral variants found in the mother An important but unanswered question is whether disease progression is more rapid in infants infected with multiple versus single HIV variants. In a pilot project, we tested the hypothesis that simultaneous infection of rhesus infants with a pathogenic simian immunodeficiency virus (SIV) and a virulence-attenuated chimeric virus (containing the HIV-1 envelope in an otherwise SIV genome) designated SHIV, would result in persistent, low viremia in peripheral blood and delayed disease progression compared with macaques (historical controls) infected with only pathogenic SIV or only with non-pathogenic SHIV. Four neonatal rhesus macaques were inoculated intravenously with a mixture of SIV and SHIV. All animals had persistently high virus levels in peripheral blood throughout the experiment and were euthanized with clinical signs of disease by 14 weeks after inoculation. This high viremia and rapidly fatal disease also resulted in macaques infected with SIV only. Thus, the results of this study show that disease progression is not modulated in macaques infected with multiple viral variants, one of which is virulence-attenuated. *KEY* Pediatric simian AIDS, Coinfection, Attenuated viral variant